Neurochemical research
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Neurochemical research · Dec 2000
Calcium sequestering ability of mitochondria modulates influx of calcium through glutamate receptor channel.
The excitotoxicity of glutamate is believed to be mediated by sustained increase in the cytosolic Ca2+ concentration. Mitochondria play a vital role in buffering the cytosolic calcium overload in stimulated neurons. Here we have studied the glutamate induced Ca2+ signals in cortical brain slices under physiological conditions and the conditions that modify the mitochondrial functions. ⋯ To validate this, influx of Mn2+ through ionotropic glutamate receptor channel was monitored by measuring the quenching of Fura-2 fluorescence. Treatment of slices with oligomycin and rotenone prior to glutamate exposure conspicuously reduced the rate of glutamate induced fluorescence quenching as compared to untreated slices. Thus our data establish that the functional status of mitochondria can modify the activity of ionotropic glutamate receptor and suggest that blockade of mitochondrial Ca2+ sequestration may desensitize the NMDA receptor operated channel.